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About HickOnACrick

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  1. Sad day. In spite of our best efforts, we have been unable to get this baby to ventilate and oxygenate. This morning, on a MAP of 10.5, this was the CXR: Last night we tried a mixture of milrinone and dobutamine to increase cardiac output and open the pulmonary vascular bed, but this made our oxygenation and ventilation worse. We stopped those meds and the baby did fairly well overnight with respect to his blood gases, and we were able to wean the amplitude somewhat. The echo yesterday showed a small PFO shunting left to right, but otherwise, no significant pathology. Throughout the morning and the afternoon, his oxygen saturation and ventilation worsened, necessitating we increase his amplitude to levels higher than last night. This was a CXR from the early evening: As compared to yesterday, the PIE has gone from micro to macro, and the hyperexpansion remains in spite of modest MAPs. This CXR was on a MAP of 11, amplitude of 32 and a Hz of 6. Baby was on 100% FiO2 and saturations were in the 60s. During the course of this disease process, I have been retrospectively reviewing the train of events. The mother was admitted with bulging bags at 23 weeks gestation, and in labor. Her labor was stopped with MgSO4 and indocin. She received a full course of betamethasone and was started on antibiotics soon after admission. Baby delivered vaginally a week later, within intact membranes and was intubated in the delivery room. All resuscitation was performed, surfactant administered, lines in place, antibiotics started, and the top of the isolette was down within 60 minutes. Looking at the PiPs, they dropped to low 20s after surfactant, but then began rising again at about 16 hrs of life. The FiO2 was between 21-25% during this time and the MAPs on volume-targeted ventilation (5 mL/kg) remained at around 7 mmHg. PEEP was at 5 mmHg. At 16 hrs of life, the PiPs climbed to the high 20s/low 30s. Because the supplemental FiO2 need was minimal, a second dose of surfactant was not given. Retrospectively, I can see evidence of PIE as early as the second day of life. My question today was: should we be basing our administration of surfactant less on FiO2 and MAPs and more on PiPs? Any thoughts?
  2. Here is the CXR when the baby's MAP was 12: Here is the CXR when the MAP was 8: Clearly the hyperexpansion and air trapping are much worse on the second CXR with a lower MAP. Per @Miguel Pantoja we increased the MAP from 8 to 10 and have now weaned to 80% with SpO2 in the low 90s. We will continue to wean FiO2 until we reach a nadir, then slowly increase the MAP to a maximum of 12, while trying to wean the amplitude, then we will try and be patient and let the lungs heal if oxygenating and ventilating reasonably well. Ideally, I would like to get the amplitude to no more than 2x the MAP. I have a CXR ordered for the early morning and will try and post it hear to show the difference. Truly thankful for everyone who has contributed to this thread.
  3. We started steroids 5 days ago, albeit the low-dose DART protocol of dexamethasone. I am about to start Milrinone and dobutamine to improve cardiac function. Thanks for your input.
  4. We got the Hz down to 6, but our first attempt to wean the amplitude resulted in a pretty significant respiratory acidosis. What is really strange is that in spite of weaning the MAP from its original 14 to now 8, the hyperexapnsion by CXR is getting worse. I speculate that the air leak is not healing at all, and we essentially have thousands of little tension pneumothoraces surrounding what little areas of gas exchange the baby has; I wouldn't really call them alveoli at 24 weeks. Awaiting an echo now to assess shunting and see if an argument can be made to increase contractility with milrinone.
  5. You may already be doing all of the following, but these are some of the things we do to prevent CLABSI: 1. TPN changes are performed as a sterile procedure; nobody is allowed within 10 feet of the bedspace without hat and mask. The RN doing the change is gowned up, hat, mask and sterile gloves. Of course, new tubing with every change of TPN 2. Standardized feeding guidelines to prevent days with a CVL in place 3. Minimizing breaks into the line for medications. Medications such as caffeine are changed to po as soon as baby demonstrates ability to tolerate po feeds (at about 60 mL/kg/day) 4. Changing from a UVC to what we call a "midline" if we anticipate the need for access beyond 5 days. A midline uses the same equipment/procedure as a PICC, but is not inserted all the way into a central vein. We treat theses as PIVs with respect to osmolarity/osmolality of TPN. Our last CLABSI was a baby who had a mild bloodstream infection which we identified as the same clone of bacteria we found in mother's EBM, but since the baby had a CVL in place, it was classified as a CLABSI - this was last year. We are not a huge NICU, but in general, about 30% of our census has had a CVL in place at some time. Based on our VON reporting, we regularly go more than one year without a reported CLABSI.
  6. Thank you everyone for your input. In spite of continuing to lower the MAP, the CXR remains hyperexpanded. Base deficit slowly worsened throughout the day, although BP remained acceptable. The Hct is stable at 45%. I gave 20/kg of isotonic bicarbonate last night for a base deficit of -10, and the pH and base deficit improved. Awaiting another CXR this morning, if it still looks hyperexpanded, I will focus more on decreasing Hz. There seems to be some disagreement in what limited literature I can find (mostly opinions) as to whether a Hz of 12-15 or Hz of 6-9 is more beneficial. Anecdotal only, but this baby seems to be responding better to the low Hz strategy. I will get a bit more aggressive about lowering Hz today, then maybe I can start weaning the amplitude as I speculate it may be the culprit of hyperexpansion. I have used the HFJV in the past to manage PIE, with good results, certainly a much more rapid response than the current case I am managing. However, at my current facility, we do not have a HFJV. Also, we are using the SensorMedics HFOV, which to my knowledge, does not have the ability to do HFOV+VG. As to repositioning the baby, we tried this earlier this week with abysmal results. Repositioning on the SensorMedics HFOV is very difficult. I will give an update in an hour or two.
  7. Over the past 3 hours, I have slowly weaned the MAP from 11 to 9. FiO2 has remained 80-90% while SpO2 has been 88 - 91%. Blood gas prior to weaning was 7.31/42/41/21/-5 and the CXR still looked hyperexpanded at a MAP of 11. Most recent gas on MAP 9, Amplitude of 38 and Hz of 9.5 was 7.13/69.6/45/23/-6, 90% FiO2 and 90% SpO2. I dropped the Hz by 0.5 but left all other parameters as they were. Although the base deficit is slowly worsening, he has brisk capillary refill, is urinating briskly, and is maintaining MBPs >32 mmHg without vasopressors or inotropes, thus his delivery of oxygen has not been severely compromised by accepting lower SpO2.
  8. I took over the care of a 24 weeker who developed PIE at about 5 days of life. Baby was doing well on conventional vent (volume-targeted ventilation), when at day 3 their oxygenation and ventilation began worsening. By day 5, PiPs were in the high 20s/low 30s. By day 6, the decision was made to change to HFOV. Our attempts to wean MAP while keeping SpO2 >88% were unsuccessful. We were able to get the MAP from 18 down to 14, but attempts to wean lower resulted in worsening oxygenation. At DOL 7, I made the decision that unless we could get the PIE to resolve, we were likely going to lose the baby, so I changed the strategy. Weaning the MAP became the primary concern at the expense of FiO2 and SpO2. I am accepting SpO2 in the 80s and 100% FiO2. I am allowing hypercarbia as long as the pH is >= 7.25 and pCO2 is < 70. This has required a higher amplitude and lower Hz than I would like, but it seems to be working. Do any of you have specific experience in treating PIE with HFOV? If so, what worked and what didn't work? How did you manage the Hz/frequency? I will give an update later today.
  9. We use a calculation of Total Fluid per day (on day zero) based on birthweight. <750 gram = 120 mL/kg/day 750 - 1000 grams = 100 mL/kg/day 1000 - 2000 grams = 80 mL/kg/day >2000 grams = 60 mL/kg/day For us, total fluids DOES NOT include medications, flushes and boluses/transfusions, rather we have guidelines in place to minimize extra fluid in medications and flushes, and we are very judicious with respect to boluses/transfusions. We increase total fluid by 20 mL/kg/day, assuming no edema. Whenever possible, we convert IV medications to po to avoid excess flushes (and also decrease risk of CLABSI). For example, we convert caffeine to po once the baby reaches 60 mL/kg/day of enteral feeds. Our Total Fluid goal on preterm babies is 160 mL/kg/day. On term babies it is 150 mL/kg/day. We consider insensible losses to be 60 mL/kg/day for patients with oliguric renal disease. Rarely do we exceed 160 mL/kg/day of total fluid on any baby unless there are weight gain issues, with fortified feeds, in the absence of respiratory/cardiac compromise. As I have gained experience, I rarely follow daily electrolytes, unless there is evidence of excessive weight loss, weight gain, poor urine output, or IV fluids lacking electrolytes. Essentially, I consider the kidneys to be smarter than me. Too often I see Neos getting daily electrolytes; on Monday they increase the Na, Tuesday they decrease the Na, increase the K, fudge the Ca, Wednesday they increase the Na, decrease the K, fudge the Ca, etc, etc, etc. At the end of the week, the baby has had 10% of their blood volume removed because of "tinkeritis". Labs beget labs, then they beget blood transfusions. We consider birthweight the calculable weight until the baby exceeds the birthweight, without signs of edema. Fluid restriction has no evidence to promote the closure of a PDA, and as long as total fluid is < 180 mL/kg/day, I have found no evidence that excess fluid volumes increase the length of time to close the PDA and affect respiratory status. In my readings/experience, PDA closure is more about minimizing inflammation, rather than fluid balance. We are strong advocates of enteral feeds and human-milk products vs. bovine-milk products. All the best!
  10. Was there a transient improvement in SaO2 and FiO2 after surfactant administration, say for 2-4 hours? If so, I would consider a surfactant protein mutation such as heterogenous SPB mutation or homogenous/heterogenous ABCA3 mutation. Also SPC mutations are highly variable in their presentation(s). Homogenous SPB mutations may have a brief response to surfactant, but will inevitably return to a severe RDS clinical picture. Heterogeneous SPB mutations may be survivable if the baby is full term. Heterogeneous ABCA3 mutations are survivable if not premature while homogenous ABCA3 mutations are often fatal, even in full-term babies. Recommend searching papers by N. Nogee and A. Hamvas Another thought, the penetration of the Xrays may not have been optimized for the type of CXR; thus the CXR looks abnormal while the CT is normal. Does the "whiteness" of the stomach bubble correspond to the "whiteness" of the lung? if so, the CXR was probably under penetrated. if the stomach bubble is much blacker than the lung fields, there is a problem with the lungs.
  11. Who needs an electronic nose when dogs and/or pigs could be trained to detect the same differences in VOCs? That is some point of care testing, although I suspect it would not be bedside. I am being a bit facetious, we have cut our NEC rate to nearly zero with a standardized feeding protocol including the addition of Prolacta. We are currently assessing whether the cost of Prolacta warrants its continued use, but from the 45,000 foot view, I suspect it will show a cost benefit. Thanks for the interesting article(s).
  12. I queried one of my RTs this week, asking, "why are they not using HFOV as a lung protective strategy?" Essentially the answer was that HFOV is considered a rescue ventilator mode, and once they are on HFOV, they are calling for ECMO. The adult ICUs are using Vt of ~5mL/kg, but the PEEPs and PiPs to achieve that Vt is astonishing. Done properly, HFOV need not be a rescue therapy. With the increased focus on really good neonatal ventilators, especially those that can reliably provide volume-targeted support for babies < 1000g, I find myself using HFOV less and less. However, if my options were a PEEP of 20 (realistically 7 in neonate) or HFOV, I would opt for the HFOV every time.
  13. To answer my own question (5) https://www.frontiersin.org/articles/10.3389/fped.2020.00206/full#B16 It is mostly speculation by the authors, but very interesting nonetheless
  14. During Covid-19, I have spent more time researching Adult pulmonary critical care than Neonatal pulmonary critical care. Based on this blog: https://emcrit.org/category/pulmcrit/ I am both fascinated and disgusted by the approach to respiratory support for Covid-19 patients. For those that have been following adult pulmonary critical care: 1. Are you appalled by the PEEP and PiPs? 2. Are you appalled by the FiO2s? 3. Do you feel like this is Neonatology circa 1990? 4. Do you think HFOV and/or NBCPAP are tools that should be applied earlier, not later for Covid-19 patients? 5. Do you have a hypothesis as to why neonates, who are inherently immunocompromised, are not more severely affected? Thank you
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